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Summary Pathology of the Gastrointestinal tract and its accessory organs
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  • Course
  • Pathology (PATHO)
  • Institution
  • Poznan University Of Medical Sciences
  • Book
  • Robbins & Cotran Pathologic Basis of Disease

This documents present in very organized and easily accessible way all of the informations and details you need to know about diseases associated with the gastrointestinal tract, the gallbladder, and the pancreas. It contains all the informations and images present in Robbins and Cortan Pathologic ...

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Document information

  • No
  • The liver, the gallbladder, the pancreas, the gastrointestinal tract
  • April 4, 2022
  • 6
  • 2021/2022
  • Summary

Subjects

  • medicine
  • pathology
  • liver
  • gallbladder
  • pancreas
  • gatrointestinal
  • esophagus
  • stomach
  • intestine
  • disease
  • illness
  • symptoms

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  • Poznan University of Medical Sciences
  • Pathology (PATHO)
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The Pancreas
[Congenital anomalies]


PANCREATITIS
 Mechanisms that normally protect the pancreas from self-digestion
o Enzymes secreted as inactive proenzymes (zymogens)
o Activation of proenzymes in the small intestine, not the pancreas
 Enterokinase (duodenal enteropeptidase)  activates trypsin in the small
intestine  activates zymogens
o Acinar and ductal cells secrete trypsin inhibitors (serine protease inhibitor Kazal type 1)
 Pancreatitis: deranges protective mechanisms  pancreas autodigestion

ACUTE PANCREATITIS
 Inappropriate activation of pancreatic enzymes  reversible pancreatic parenchymal injury and
tissue destruction, and acute inflammation reaction
 Intrapancreatic trypsin activation 
o Prophospholipase activation  fat cells degradation
o Proelastase activation  damage of elastic fibers of blood vessels  rupture
o Prekallikrein activation
o Coagulation factor XII activation  clotting (thrombosis) and complement system
 Mechanisms of pathogenesis
o Pancreatic duct obstruction
 Mainly gallstones and biliary sludge
 Periampullary neoplasms (pancreatic cancer), choledochoceles (congenital cystic
dilation of common bile duct), parasites (Ascaris lumbricoides and Clonorchis
sinensis), pancreas divisum
 Obstruction  increase intrapancreatic ductal pressure  enzyme-rich fluid
accumulation in interstitium, contains lipase (normally secreted in active form)
 local fat necrosis  signals from necrotic adipocytes  inflammatory
mediators release from periacinar myofibroblasts and leukocytes 
inflammation and edema  impaired blood flow  acinar cells ischemia
o Primary acinar cell injury
 Caused by
 Oxidative stress  free radical generation  membrane lipid oxidation
and transcription factors activation (AP1 and NF-kB)
 Increased calcium influx  autoinhibition  no more trypsin
inactivation and cleavage  trypsinogen to trypsin
o Defective intracellular transport of proenzymes within acinar cells
 Defect  transport of digestive proenzymes and lysosomal hydrolases together
(normally separate)  proenzymes activation  lysosomes disruption and
enzymes release
 Alcohol consumption
o Causes secretion of protein-rich pancreatic fluid  protein plugs deposition  small
pancreatic ducts obstruction

, o Causes oxidative stress on acinar cells  free radicals generation, lysosomes and
zymogens granules fusion, and mitochondrial damage ( increase intracellular calcium)
 Other causes: metabolic disorders (hypertriglyceridemia, hypercalcemia, hyperparathyroidism),
genetics, medications (estrogens, furosemide), infections (mumps)
 Hereditary factors: cause recurrent attacks of severe acute pancreatitis in childhood  chronic
pancreatitis
o Mutations  increased and sustained trypsin activity
o Genes: PRSS1 (trypsinogen gene gain-of-function, autosomal dominant), SPINK1 (trypsin
inhibitor loss-of-function, autosomal recessive), and CFTR (causes decrease bicarbonate
secretion by pancreatic ductal cells  protein plugging and duct obstruction)
o Increased risk of pancreatic cancer
 Basic alterations
o Microvascular leak and edema
o Fat necrosis
o Acute inflammation
o Pancreatic parenchyma destruction
o Blood vessels destruction and interstitial hemorrhage
 Acute interstitial pancreatitis
o Milder form
o Mild inflammation, interstitial edema, focal areas of fat necrosis in pancreas and
peripancreatic fat (released fatty acids + calcium  insoluble salts: blue granules in cells)
 Acute necrotizing pancreatitis
o More severe form
o Necrosis of acinar and ductal cells, and islets of Langerhans
o Vascular injury  hemorrhage
o Macroscopically: red-black (hemorrhage) with interspersed foci of yellow-white (fat
necrosis)
o Fat necrosis in pancreas, omentum and mesentery of the bowel, and outside the
abdominal cavity (subcutaneous fat)
o Peritoneal cavity contains serous, turbid, brown-tinged fluid with globules of fat
 Hemorrhagic pancreatitis
o Most severe form
o Extensive parenchymal necrosis
o Hemorrhage within the gland
 Symptoms:
o Abdominal pain in the upper back and left shoulder
o Elevated serum amylase in first 24 hours
o Elevated serum lipase in 72 – 96 hours
o Glycosuria, hypocalcemia (calcium soap precipitation in necrotic adipocytes)
o Enlarges pancreas on CT scan
 Full-blown acute pancreatitis
o Medical emergency
o Sudden onset of an “acute abdomen”
o Systemic inflammatory response: leukocytosis, DIC, edema, and ARDS  shock
 Treatment: total restriction of oral intake, with supportive IV fluids and analgesia
 Complications: ARDS and acute renal failure, sterile pancreatic abscess and pancreatic
pseudocyst, infection with enteric gram (-) bacteria

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